Acidic HEPES-KH Reperfusion Enhances Myocardial Protection in Immature Rabbits

Summary: To study the effects of different pH HEPES-KH reperfusate solution on immature myocardial protection, isolated perfused Langendorff model from immature rabbit hearts were developed formed. Control group (C) was perfused only with pH 7. 4 HEPES-KH solution for 90 min. Is chemia/reperfusion group (group I/R) was perfused with pH 7. 4 HEPES-KH solution before is chemia or after ischemia. Experimental group (group E), after ischemia, was perfused with pH 6.8,pH 7. 1 and pH7.4 HEPES-KH solutions for 5 min, 5 min, and 20 min, respectively. The left ven tricular function recovery, MWC, LDH and CK leakage, MDA, ATP content, and SOD activity were determined. Our results showed that the left ventricular function recovery, ATP content and SOD activity in group E were higher than those of group I/R (P＜0. 05). MWC, MDA content,LDH and CK leakage in group E were lower than those of group I/R (P＜0. 05). These findings suggested that pH paradox might be one of important mechanisms for immature myocardial ischemia reperfusion injury, and acidic perfusate, at the beginning of reperfusion, might attenuate pH paradox and ameliorate functional recovery in isolated perfused immature rabbit hearts.     

卡立泊来德复合心脏停跳液对兔未成熟心肌的保护作用

目的 比较选择性钠氢离子交换阻断剂卡立泊来德（Cariporide）联合不同心脏停跳液（St．Thomas液与HTK液）对未成熟心肌缺血／再灌注损伤的保护作用。方法32只新西兰幼兔（2-3周龄）,建立Langendorff离体心脏灌注模型后,随机分为4组,每组8只：对照组（st组,St．Thomas液）、HTK组（HTK液）、St＋C组（St．Thomas液中添加Cariporide）和HTK＋C组（HTK液中添加Cariporide）。所有心脏均30℃全心缺血120min,37℃KH液再灌注60min。记录心功能参数：左室发展压（LVDP）、左室最大收缩变化率（＋dp／dtmax）、左室最大舒张变化率（-dp／dtmax,）及冠脉流量（CF）;测定冠脉流出液中磷酸肌酸激酶同工酶（CK-MB）、心肌三磷酸腺苷（ATP）、丙二醛（MDA）、心肌细胞内钙（iCa）及心肌含水量（WC）。结果 HTK组LVDP、＋dp／dtmax、-dp／dtmax,、CF恢复率及ATP含量均明显高于St组（P〈0．05）,CK-MB、MDA、WC和iCa明显低于St组（P〈0．05）;St＋C组、HTK＋C组各指标分别优于st组、HTK组,且HTK＋C组各指标则优于st＋C组;而st＋C组与HTK组比较显示,St＋C组-dp／dt-、CF恢复率和ATP高于HTK组（P〈0．05）,而MDA高于HTK组（P〈0．05）,其余指标两组差异无统计学意义（P〉0．05）。结论Cariporide能提高St．Thomas液及HTK液对未成熟心肌缺血再灌注损伤的保护作用。     

卡立泊来德对鼠移植供心的保护效果

目的 通过离体心脏灌流模型(Langendorff),评价卡立泊来德(Cariporide)对离体鼠移植供心的保护效果.方法 48只雄性Wistar大鼠随机分为四组.对照组两组:HTK(Histidine-Tryptophan-Ketoglurate Solution)8h、12h组,实验组(Cariporide 组)两组:HTK+Cariporide 20μmol/L,8h、12h组.切取鼠供心后即悬挂在Langendorff上灌注,测定血流动力学基础值.分别用两种器官保存液灌注离体鼠心后置于各自的冷心肌保护液(4℃)中保存8h、12h,恢复灌注后再次测定血流动力学指标和冠状动脉流量,留取标本分别测定心肌水含量、心肌酶漏出量、心肌细胞ATP含量,观察心肌细胞超微结构变化.结果 在冷缺血8h后,与对照组相比,实验组的平均左室发展压(LVDP)及心肌ATP含量均增高,磷酸肌酸激酶同工酶(CK-MB)漏出量减少,但差异无统计学意义.在冷缺血12h后,与HTK组相比,卡立泊来德组LVDP均显著升高[(98.37±16.34)mmHg、(43.21±14.33)mmHg,(P＜0.01)](1 mmHg=0.133kPa);CK-MB漏出量明显减少[(4.373±1.489)IU/L、(34.23±3.328)IU/L,(P＜0.01)];心肌ATP含量明显增多[(34.32±1.87)μg/g、(17.92±1.47)μg/g,(P＜0.01)].结论 Cariporide对离体鼠供心具有较好的保护效果,并可延长供心的低温保存时间.     

水飞蓟宾对离体心脏组织缺血再灌注损伤保护作用及机制研究

[目的]探讨水飞蓟宾（SIL）对Langendorff灌流大鼠离体心脏缺血再灌注损伤的保护作用及其作用机制。[方法]100只SD大鼠随机分为正常对照组、模型组、SIL低[100 mg/（kg·d）]、中[200 mg/（kg·d）]、高[400 mg/（kg·d）]剂量组,各20只;手术前2h灌胃给药,采用Langendorff灌流系统制备大鼠离体心脏灌注模型,模型组与SIL各组灌注K-H液20 min后停灌30 min、然后再灌注60 min后行各指标检测,而正常对照组持续灌注K-H液。测定冠脉流出液心肌酶活性;通过四氮唑（TTC）染色计算心脏组织梗死面积,采用苏木精-伊红（HE）染色对心脏组织进行病理学检查;测定血流动力学指标;测定抗氧化酶活性和丙二醛（MDA）含量;测定心肌组织Na⁺-ATPase、Ca²⁺-ATPase酶活力。[结果]与模型组比较,SIL中、高剂量组心肌酶：谷草转氨酶（AST）、乳酸脱氢酶（LDH）、肌酸激酶MB同工酶（CK-MB）活性显著降低,梗死面积显著降低;病理学检查结果显示：经SIL干预能够明显改善心脏组织病变;血流动力学指标明显改善[心率（HR）、左室收缩压（LVSP）、左室收缩压最大上升速率（+dP/dtmax）、左室舒张压最大下降速率（-dP/dtmin）显著升高,左室舒张压（LVEDP）显著降低];抗氧化酶：超氧化物歧化酶（SOD）、过氧化氢酶（CAT）活性显著升高且MDA含量显著降低;Na⁺-ATPase、Ca²⁺-ATPase酶活力显著升高,上述结果差异具有统计学意义（P<0.05或P<0.01）。[结论]SIL对离体心脏缺血再灌注损伤具有一定的抑制作用,其作用机制可能与SIL能够改善血液流变学指标、抑制氧化应激、提高ATP酶活力有关。     

去甲肾上腺素预处理对大鼠供心超氧化物歧化酶及丙二醛表达的影响

目的探讨去甲肾上腺素预处理对大鼠供心心肌细胞超氧化物歧化酶(SOD)及丙二醛(MDA)表达的影响。方法雄性Wistar大鼠18只随机分为对照组和实验组各9只,对照组腹腔注射生理盐水0.5 mL,24 h后取离体心脏灌注Histidine-tryptophan-ketoglutarate心脏保护液,4℃保存3 h后建立Langendorff离体心脏灌注模型,灌注Krebs-Henseleit液2 h;实验组腹腔注射重酒石酸去甲肾上腺素(溶于生理盐水)3.1μmol.kg-1(0.53 mg.kg-1),24 h后取离体心脏,处理方法同对照组。测定2组肌酸激酶(CK)、乳酸脱氢酶(LDH)漏出率以及心肌水含量(MWC)、SOD、MDA的水平。结果实验组SOD的水平较对照组明显升高(P<0.01);MWC、MDA含量、CK、LDH漏出率较对照组明显降低(P<0.01)。结论去甲肾上腺素预处理能促进SOD表达,降低MDA含量,对抗氧自由基损伤,从而发挥对离体大鼠供心心肌的保护效应。     

肾缺血预处理对未成熟心肌保护作用的研究

①目的　研究肾缺血预处理对未成熟心肌保护作用 ,探讨未成熟心肌保护方法。②方法　建立心脏缺血预处理 (IP)和肾缺血预处理 (RIP)兔Langendorff灌注模型。将兔随机分为 3组。缺血 再灌注组 (I R组 ) :在Langendorff模型基础上 ,灌注 15min转为工作心 15min ;IP组 :在Langendorff模型基础上 ,灌注 15min转为工作心 15min ,反复 2次缺血 5min再灌注 5min ;RIP组 :反复 3次阻断左肾动脉血流 5min再灌注 5min ,建立模型 ,灌注 15min转为工作心 15min ;然后各组全心停止灌注 4 5min ,恢复灌注 15min改为工作心 30min。以左心室功能恢复情况、心肌含水量 (MWC)、血清肌酸激酶 (CK)和乳酸脱氢酶 (LDH)漏出率、心肌组织ATP和丙二醛 (MDA)含量、超氧化物歧化酶 (SOD)活性、心肌细胞内Ca2 + 含量、心肌线粒体Ca2 + ATPase活性及其Ca2 + 含量、心肌线粒体合成ATP能力 { [ATP]m}作为观察指标。③结果　RIP组和IP组左室功能恢复百分率高于I R组 (F =4 .6 7～6 .0 3,q =2 .6 0～ 3.12 ,P <0 .0 5 ) ,RIP组和IP组比较差异无显著性 (q =1.2 3～ 1.98,P >0 .0 5 ) ;RIP组和IP组MWC低于I R组 (F =5 .6 8,P <0 .0 5 ) ,RIP组和IP组比较差异无显著性 (q =1.6 5 ,P >0 .0 5 ) ;RIP组和IP组MDA含量、CK和LDH漏出率、ATP含     

热休克蛋白70对兔未成熟心肌和心肌间质的影响

目的: 探讨热休克蛋白70(HSP70)对未成熟心肌和心肌间质的影响. 方法:健康新生长耳大白兔12只随机分为2组. 对照组(C组):ip生理盐水0.4 mL,24 h后取离体心脏,常规建立Langendorff离体心脏灌注模型,灌注15 min转为工作心15 min后停灌45 min,恢复灌注15 min改为工作心30 min;实验组(E组):ip去甲肾上腺素, 24 h后取离体心脏,方法同对照组. 测定心肌细胞中HSP70含量、血流动力学指标、心肌含水量(MWC)、心肌肌酸激酶(CK)和乳酸脱氢酶(LDH)漏出率、三磷酸腺苷(ATP)含量、超氧化物歧化酶(SOD)和丙二醛(MDA)含量、心肌组织羟脯氨酸(HP)含量、内皮素(ET) 含量、心肌细胞内Ca2 含量、心肌线粒体Ca2 -ATPase活性及其Ca2 含量、心肌线粒体合成ATP能力[ATP]m,心肌超微结构. 结果:E组HSP70含量明显高于C组(P<0.01);MWC低于C组(P<0.05);ATP含量、SOD活性、心肌线粒体Ca2 -ATPase活性、[ATP]m, HP含量优于C组(P<0.01),MDA含量、CK, LDH漏出率、心肌细胞内Ca2 含量、心肌线粒体Ca2 含量、ET含量低于C组(P<0.01),心肌超微结构损伤较C组明显减轻. 结论:HSP70对缺血再灌注未成熟心肌和心肌间质具有明显的保护作用.     

丹参多酚酸对大鼠缺血心肌线粒体酶的影响

目的:探讨丹参多酚酸对大鼠心肌缺血再灌注过程中线粒体Na+,K+-ATP酶和Ca2+-ATP酶的影响。方法:采用健康Wistar大鼠(n=40)建立Langendorff离体心脏灌注模型,并分为4组。对照组用Krebs液持续灌注120 min;缺血再灌注组平衡30 min后全心缺血30 min,再灌注60 min;丹参多酚酸预处理组平衡5 min后加入丹参多酚酸使其在灌流液中终浓度为14μmol/L,持续灌注25 min后全心缺血30 min,再灌注60 min;丹参多酚酸后处理组平衡30 min后全心缺血30 min,加入丹参多酚酸使其在灌流液中终浓度为14μmol/L,再灌注60 min。TTC染色观察心肌梗死面积,并用心肌梗死面积、乳酸脱氢酶(LDH)活性和心脏血流动力学(包括心率、主动脉流量、冠状动脉流量和心输出量)的变化评估大鼠心肌的损伤程度。利用差速离心法提取线粒体,并通过紫外分光光度法测定心肌线粒体Na+,K+-ATP酶和Ca2+-ATP酶的活性。结果:丹参多酚酸预处理组的心肌梗死面积和LDH活性均显著低于缺血再灌注组([24.47±2.14)%比(34.30±2.31)%、(81.46±13.39)U/g比(142.6±6.46)U/g,均P<0.05],缺血再灌注组与后处理组无明显差异。丹参多酚酸对缺血再灌注心肌的血液动力学没有明显作用,只是冠脉流量有较小幅度的增加。丹参多酚酸预处理组线粒体Na+,K+-ATP酶和Ca2+-ATP酶活性显著高于缺血再灌注组([6.12±0.42)U/mg比(4.29±0.28)U/mg、(3.42±0.16)U/mg比(2.62±0.96)U/mg,均P<0.05],而与对照组无明显差异。丹参多酚酸后处理组线粒体Na+,K+-ATP酶和Ca2+-ATP酶活性与缺血再灌注组无统计学差异。结论:丹参多酚酸可以维持心肌线粒体Na+,K+-ATP酶和Ca2+-ATP酶的活性,通过降低缺血再灌注对心肌线粒体的损伤保护心肌。     

乌拉坦增强延长离体大鼠心脏的低温保存效果

目的：观察乌拉坦对延长离体大鼠心脏的低温保存作用.方法：成年雄性SD大鼠分为两组（n=6）：对照组：HTK保存液; 试验组：HTK保存液加乌拉坦（30mmol/L）.心脏分别置入两种保存液4℃下保存6和18h.采用Langendorff心脏灌注装置进行保存前及保存后再灌注30min时心脏功能测定,比较心脏功能恢复率、ATP含量、细胞凋亡和超微结构变化.结果：低温保存后实验组左室功能恢复率较对照组明显升高,细胞凋亡及超微结构损伤较对照组减轻; 保存18h后实验组ATP含量显著高于对照组.结论：乌拉坦加入HTK心脏保存液能够显著增强离体大鼠心脏的低温保存效果.     

脂质体携载前列腺素E1含血停搏液对未成熟心肌的保护效果

目的：探讨脂质体携载前列腺素E1(Lipo-PGEl)加入Thcmas Ⅱ停搏液对未成熟心肌的保护效果。方法：2～3周龄新西兰大白兔20只,随机分为2组,每组10只。建立Langendoff离体心脏灌注模型。对照组：TlxxnasⅡ号停搏液灌注加低温;实验组：Lipo-PGE1加入ThomasⅡ号停搏液灌注并行低温。全心平均停循环90min,再灌注30min。观察指标：冠脉流量恢复率(CFR)、心肌丙二醛(MDA)／超氧化物岐化酶(SOD)含量、心肌三磷酸腺苷ATP含量、心肌含水量、心肌磷酸肌酸激酶(CK)漏出量和乳酸脱氢酶(LDH)漏出量。结果：再灌注末实验组心肌MDA含量低于对照组,而SOD含量高于对照组;实验组CFR和再灌注末心肌ATP含量高于对照组;实验组心肌含水量、CK和LDH漏出量低于对照组。结论：Lipo-PGE1加入含血ThcmasⅡ号停搏液可改善对未成熟心肌的保护效果。     

Phospholamban Antisense RNA Improves SR Ca2+-ATPase Activity and Left Ventricular Function in STZ-induced Diabetic Rats

ObjectiveTo study the effect of phospholamban antisense RNA (asPLB) on sarcoplasmic reticulum Ca²⁺-ATPase activity and cardiac function in rats with diabetes mellitus (DM) mediated by recombinant adeno-associated virus (rAAV) vector.MethodsSix weeks after the induction of DM by streptozotocin injected intraperitoneally, the rats were divided into three groups, namely: DM-rAAV-asPLB group, DM-saline group and DM group (control group). The rats in the DM-rAAV-asPLB group were intramyocardially injected with rAAV-asPLB, the rats in the DM-saline group were injected with saline, and those in the control group did not receive any treatment. Six weeks after gene transfer, the expressions of PLB protein and PLB phosphorylation were detected by Western-blot, while the activity of sarcoplasmic reticulum (SR) Ca²⁺-ATPase and left ventricular function were measured.ResultsThe PLB protein expression level was significantly higher whereas the PLB phosphorylation, SR Ca²⁺-ATPase activity and left ventricular function were significantly lower in the DM-saline group than in the control group. No significant difference was found in PLB protein expression level, PLB phosphorylation or SR Ca²⁺-ATPase activity between the DM-rAAV-asPLB group and the control group. The left ventricular function in the DM-rAAV-asPLB group was poorer than in the control group and was better than in the DM-saline group.ConclusionrAAV-asPLB can down-regulate PLB protein expression and up-regulate PLB phosphorylation and SR Ca²⁺-ATPase activity, thus contributing to the improvement of in vivo left ventricular function.     

Effect of Huoxuequyu recipe on erythrocyte membrane Ca2+-ATPase activity in pregnant rats with asymmetrical intrauterine growth retardation induced by passive smoking

Summary The effect of Huoxuequyu recipe on erythrocyte membrane Ca²⁺-ATPase activity in pregnant rats with passive smoking induced asymmetrical intrauterine growth retardation (IUGR) was observed. The rats were divided into three groups: control group, model group and treated group. The fetal mean birth weight and erythrocyte membrane Ca²⁺-ATPase activity were found to be decreased in the model group as compared with the control and treated groups. There was a significant difference between the model group and the control group (P<0.01), while no significant difference existed between the treated group and the control group (P>0. 05). Furthermore, the findings indicated that the erythrocyte membrane Ca²⁺-ATPase activity seem to be positively correlated with the birth weight (P<0. 05). On the basis of our observation, it is believedthat the Huoxuequyu decoction could increase erythrocyte membrane Ca²⁺-ATPase activity and promote blood circulation, thereby exerting a beneficial effect on fetal development. This project is supported by the National Natural Sciences Foundation of China. No 39270826     

银杏二萜内酯葡胺注射液对离体心脏缺血再灌注损伤保护作用的实验研究

[目的]研究银杏二萜内酯葡胺注射液（DGMI）对大鼠离体心脏缺血再灌注损伤的保护作用并探讨其机制。[方法]取120只SD大鼠随机分为正常对照组、模型组、DGMI低（1.5 mg/kg）、中（3 mg/kg）、高（6 mg/kg）剂量组和维拉帕米2.5 mg/kg组（阳性药物对照组）,各20只;手术前2 h,腹腔注射给药,正常对照组和模型组同步给予生理盐水。采用Langendorff灌流系统建立离体心脏灌注模型,正常对照组持续灌注Krebs-Henseleit液（K-H液）,模型组、DGMI各剂量组和维拉帕米组平衡灌注20 min后停灌30 min、再灌注60 min后行各指标检测。测定冠脉流出液心肌酶活性;2,3,5-氯化三苯基四氮唑（TTC）染色测定心脏组织梗死面积,苏木精-伊红（HE）染色观察心脏组织病变;测定血流动力学指标;测定心肌组织中抗氧化酶活性以及丙二醛（MDA）含量;测定心肌组织ATPase活力。[结果]与模型组比较,DGMI中、高剂量组和维拉帕米2.5 mg/kg组大鼠血清心肌酶谷草转氨酶（AST）、乳酸脱氢酶（LDH）和肌酸激酶MB同工酶（CK-MB）活性均显著降低（P<0.05或P<0.01）;心脏组织梗死面积显著降低（P<0.01）,心脏组织病变明显改善;明显改善血流动力学指标：心率（HR）、左室收缩压（LVSP）、左室收缩压最大上升速率（+dP/dt_max）、左室舒张压最大下降速率（-dP/dt_min）均显著升高且左室舒张末压（LVEDP）显著降低（P<0.05或P<0.01）;抗氧化酶[超氧化物歧化酶（SOD）、过氧化氢酶（CAT）]活性显著升高且MDA含量显著降低（P<0.05或P<0.01）;Na⁺-ATPase、Ca²⁺-ATPase酶活力显著升高（P<0.05或P<0.01）。[结论]DGMI可能通过改善血液流变学、降低氧化应激损伤、改善ATPase活力而对大鼠离体心脏表现出一定的保护作用。     

褪黑素通过抑制挛缩减轻大鼠离体心脏的缺血再灌注损伤

目的 探讨褪黑素（Mel）抑制挛缩改善大鼠离体心脏缺血再灌注（IR）损伤的作用及机制。方法 采用Langendorff离体心脏灌流方法模拟缺血再灌注模型,40只SD大鼠按随机数字表法分为4组（10只/组）。正常对照组（Control）：正常灌注175 min;IR组：全心缺血45 min,再灌注120 min;Mel+IR组：用Mel（5 μmol/L）灌注1 min,全心缺血45 min,用Mel（5 μmol/L）再灌注5 min,Krebs-Henseleit液再灌注115 min;挛缩抑制剂2,3-丁二酮单肟（BDM）干预缺血再灌注组（BDM+IR）：用BDM（20 mmol/L）灌注1 min,全心缺血45 min,用BDM（20 mmol/L）再灌注5 min,KH液再灌注115 min。以心肌死亡面积、caspase-3活性、细胞色素c（cytochrome c）和cleaved caspase-3蛋白表达检测各组心肌损伤程度;以HE染色、冠脉流出液中乳酸脱氢酶（LDH）活性、肌钙蛋白（I cTnI）含量、左心室舒张末压（LVEDP）和电镜观察肌原纤维收缩带的形成评价各组心脏挛缩程度;检测心肌组织中ATP含量的变化。结果 与Control组相比,IR组心肌死亡面积、caspase-3活性、cytochrome c和cleaved caspase-3蛋白表达显著增加（P<0.01）;同时,冠脉流出液中LDH活性和cTnI含量明显增加,再灌注末LVEDP显著抬升,HE染色显示心肌纤维发生明显断裂,ELISA检测发现ATP含量显著降低（P<0.01）;另外,透射电镜结果表明IR组肌节过度收缩,形成明显的肌原纤维收缩带;而给予Mel和BDM处理后,可显著减小心肌死亡面积、aspase-3活性、cytochrome c和cleaved caspase-3蛋白表达,还可明显抑制LDH活性、cTnI含量和LVEDP,减少心肌纤维断裂,并增加胞内ATP含量;更为重要地是,Mel和BDM能减轻IR引起的肌节过度收缩,并抑制收缩带的形成。结论 Mel可通过抑制挛缩明显改善心肌缺血再灌注损伤,其机制可能与增加心肌细胞内ATP含量,减轻心肌机械性损伤引起的肌膜撕裂,减少细胞内容物的漏出有关。     

The protective effect of propofol on erythrocytes during cardiopulmonary bypass

Cardiopulmonary bypass ( CPB) can cause ery-throcytes damage.The damaged erythrocytes notonly result in hemotocytolysis and also obstruct mi-crocirculation. Recently some studies demonstratedthat Ca2 is a major factor to maintain erythrocytemembrane homeostasis and normal deformity[1] .Propofol is a rapid acting intravenous anesthetic,which possesses the properties to scavenge free radi-cals and block Ca2 channels.While whether propo-fol is effective or not in protecting erythrocytes fro…     

晶体停搏液中钙离子浓度对幼兔未成熟心肌的保护作用

OBJECTIVE: To determine the myocardial protective effect of St. Thomas II cardioplegia at different calcium concentration on immature myocardium. METHODS: Isolated perfused neonatal rabbit hearts from three groups (the calcium concentration of St. Thomas II cardioplegia was modified: [Ca2+] 0.6 mmol/L; [Ca2+]1.2 mmol/L; [Ca2+]2.4 mmol/L) were subjected to 20 degrees C hypothermia, 90 minutes of global ischemia followed by 30 minutes reperfusion in Langendorff mode. RESULTS: Although the recovery of LVDP, +/- dp/dtmax at calcium content of 2.4 mmol/L after 10 minutes of reperfusion was significantly higher than that at 0.6 and 1.2 mmol/L calcium (P < 0.05, P < 0.01, respectively), the declined tendency of left ventricular hemodynamics in this group was detected after 20 minutes of reperfusion. By the end of 30-minute reperfusion, the left ventricular hemodynamic recovery at 2.4 mmol/L calcium did not differ from those at 0.6 mmol/L and 1.2 mmol/L calcium. Conversely, postischemic left ventricular functions at 0.6 and 1.2 mmol/L calcium were gradually improved during the 30 minutes reperfusion. Ca(2+)-ATPase activity at 2.4 mmol/L calcium showed significant increase (P < 0.01, P < 0.001), whereas ATP content was lower than that of other groups. CONCLUSION: Calcium accumulated in extracellular space during ischemia enters myocardial cell via Ca2+ channel and Ca2+/Na+ exchange after reperfusion, activates Ca(2+)-ATPase, and finally accelerates adenosinetriphosphate (ATP) consumption induced by calcium, which would be responsible for the results of our study. We conclude that, from the point of view of myocardial cell energy metabolism, St. Thomas II cardioplegia at high calcium concentration can not provide immature myocardium with optimal myocardial protection.     

EFFECTS OF GLIBENCLAMIDE, GLIMEPIRIDE, AND GLICLAZIDE ON ISCHEMIC PRECONDITIONING IN RAT HEART

Objective To compare the influence of different sulfonylureas on the myocardial protection effect of ischemic preconditioning (IPC) in isolated rat hearts, and ATP-sensitive potassium channel current (IKATP) of rat ventricular myocytes. Methods Isolated Langendorff perfused rat hearts were randomly assigned to five groups: (1) control group, (2) IPC group, (3) IPC glibenclamide (GLB, 10 μmol/L) group, (4) IPC glimepiride (GLM, 10 μmol/L) group, (5) IPC gliclazide (GLC, 50 μmol/L) group. IPC was defined as 3 cycles of 5-minute zero-flow global ischemia followed by 5-minute reperfusion. The haemodynamic parameters and the infarct size of each isolated heart were recorded. And the sarcolemmal IKATP of dissociated ventricular myocytes reperfused with 10 μmol/L GLB, 1 μmol/L GLM, and 1 μmol/L GLC was recorded with single-pipette whole-cell voltage clamp under simulated ischemic condition. Results The infarct sizes of rat hearts in IPC (23.7%±1.3%), IPC GLM (24.6%±1.0%), and IPC GLC (33.1%±1.3%) groups were all significantly smaller than that in control group (43.3%±1.8%; P<0.01, n=6). The infarct size of rat hearts in IPC GLB group (40.4%±1.4%) was significantly larger than that in IPC group (P<0.01, n=6). Under simulated ischemic condition, GLB (10 μmol/L) decreased IKATP from 20.65±7.80 to 9.09±0.10 pA/pF (P<0.01, n=6), GLM (1 μmol/L) did not significantly inhibit IKATP (n=6), and GLC (1 μmol/L) decreased IKATP from 16.73±0.97 to 11.18±3.56 pA/pF(P<0.05, n=6). Conclusions GLM has less effect on myocardial protection of IPC than GLB and GLC. Blockage of sarcolemmal ATP-sensitive potassium channels in myocardium might play an important role in diminishing IPC-induced protection of GLM, GLB, and GLC.     

缺血预处理对大鼠心肌三磷酸腺苷含量及钠-钾-三磷酸腺苷酶活性的影响

目的探讨缺血预处理后心肌细胞膜钠-钾-三磷酸腺苷酶（Na^＋-K^＋-ATPase）活性变化及此变化对心肌能量消耗的影响。方法建立离体大鼠心脏灌注模型，预处理组采用5min缺血和10min灌注，反复3次，之后两组心脏应用停跳液灌注使心脏停跳，随后给予120min缺血和30min再灌注。实验过程中监测HR、dp／dt、LVDP和漏出液量，灌注结束时，取心肌标本测定心肌ATP含量和Na^＋-K^＋-ATPase活性。结果缺血再灌注过程中预处理组Na^＋-K^＋-ATPase活性明显高于对照组（P〈0．05）。预处理组心肌缺血过程中ATP消耗明显减少。结论缺血预处理使心脏在其后较长时间的缺血过程中能量消耗减少，并保护心肌Na^＋-K^＋-ATPase活性。     

酒石酸布托啡诺后处理对离体大鼠心肌缺血再灌注损伤的影响

目的探讨酒石酸布托啡诺后处理对大鼠离体心肌缺血再灌注损伤的影响。方法应用Langendorff离体灌流装置,采用完全停灌复灌的方法制作离体大鼠心肌缺血再灌注模型。健康雄性sD大鼠32只,体重220～250g,随机分为4组：对照组（Sham组,n=8）、缺血再灌注组（I／R组,n=8）、缺血预处理组（pre组,n=8）和酒石酸布托啡诺后处理组（butor组,n=8）。制备大鼠离体心脏缺血再灌注损伤模型,于再灌注结束后,收集冠脉流出液测定肌酸激酶（CK）和乳酸脱氢酶（LDH）的活性,测定心肌组织丙二醛（MDA）含量和超氧化物歧化酶（SOD）活性。结果与Sham组比较,其他各组冠脉流出液CK和LDH活性及心肌组织MDA含量升高,心肌组织SOD活性降低（P〈0．01）;与I／R组比较,pre组及butor组冠脉流出液CK和LDH活性及心肌组织MDA含量降低,心肌组织SOD活性升高（P〈0．01）,而pre组与butor组比较,CK和LDH活性及心肌组织MDA含量和SOD活性差异无统计学意义（P〉0．05）。结论酒石酸布托啡诺后处理对离体心脏缺血再灌沣榻伤具有保护作用。     

旋覆代赭汤及其拆方对RE大鼠血浆Na+-K+-ATP酶及Ca2+-Mg2+-ATP酶活性的影响

[目的] 探讨反流性食管炎(RE)食管黏膜血浆细胞能量代谢与黏膜损伤的关系以及旋覆代赭汤治疗RE的作用机制。[方法] 将120只Wistar大鼠按照随机数字法随机分为10组,每组12只,即正常组、模型组、旋覆代赭汤全方组(全方组)、苦降组、甘升组、升降相因组、去苦降组、去甘升组、去升降相因组和西药组;除正常组外,其余9组行"4.2 mm幽门夹+胃底2/3结扎术"造模。治疗14 d后,即造模后第22天处死,检测各组大鼠血浆Na⁺-K⁺-ATP酶及Ca²⁺-Mg²⁺-ATP酶的活性。[结果] 实验后各模型组大鼠ATP酶活性低于正常组;全方组、西药组酶活性较好,与正常组差异无统计学意义(P>0.05),与模型组相比有统计学差异(P<0.05);苦降组及去甘升组与模型组相比,差异无统计学意义(P>0.05),与全方组及西药组比较差异有统计学意义(P<0.05);正常组与其他各组比较,均有统计学差异(P<0.05);西药组与全方组比较,差异无统计学意义。[结论] 旋覆代赭汤全方组能提高模型大鼠血浆Na⁺-K⁺-ATP酶及Ca²⁺-Mg²⁺-ATP酶的活性,改善模型大鼠食管黏膜组织形态学病变,且作用优于各拆方组。